DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for lymph node palisaded myofibroblastoma — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleLymph node palisaded myofibroblastoma maps to a 1-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for lymph node palisaded myofibroblastoma is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
catenin beta 1 (CTNNB1) — CTNNB1 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet prodrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8Z10 · 2.35 Å · ligand PROLINE (PRO). Experimental structure, not a prediction.
What the evidence adds up to
Intranodal palisaded myofibroblastoma is a benign, lymph node-based myofibroblastic tumour of unknown pathogenesis. A 2014 study of 18 patients (14 men, 4 women, mean age 47) found tumours arose mostly in inguinal lymph nodes (15 of 18), with a mean size of 3.1 cm. Most presented with a painless mass. Histologically, the tumours showed nuclear palisades (16 of 18), collagenous bodies (15 of 18), and perinuclear intracytoplasmic hyaline globules (10 of 18). Mitotic activity ranged from 0 to 8 mitotic figures per 50 high-powered fields, with no atypical division figures. Immunohistochemically, all tested tumours expressed smooth muscle actin and/or muscle-specific actin, and nuclear β-catenin and cyclin D1. Mutations in the β-catenin gene exon 3 were identified in 7 of 8 (88%) analysed tumours, suggesting mutational activation of β-catenin is likely a pivotal event in pathogenesis.
A 2016 case report described an 84-year-old woman with Parkinson’s disease who presented with a left inguinal mass diagnosed as intranodal palisaded myofibroblastoma via ultrasound-guided fine needle aspiration biopsy and cytopathological examination including immunohistochemistry. The authors concluded the diagnosis is possible with cytopathologic exam and immunohistochemical analysis using ultrasound-guided FNA, guiding clinicians to nodal excision rather than aggressive measures.
A separate 2016 study on myofibroblasts in odontogenic cysts and tumours found that ameloblastoma showed the highest number of myofibroblasts, dentigerous cysts the lowest, and that myofibroblast counts correlated positively with known biologic behaviour of the lesions. This study did not involve intranodal palisaded myofibroblastoma.
No drug treatment is mentioned in any of these abstracts. What is missing is any clinical trial data, any drug intervention, any patient stratification beyond histologic and genetic characterisation, and any funding for therapeutic development for this rare benign entity.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
The American Journal of Surgical Pathology · 2014 · 37 citations · open access
Intranodal Palisaded Myofibroblastoma
AbstractIntranodal palisaded myofibroblastoma is a benign, lymph node-based myofibroblastic tumor of unknown pathogenesis. We report the clinicopathologic, immunohistochemical, and molecular genetic features of this rare entity. The study cohort consisted of 14 men and 4 women ranging in age from 31 to 65 (mean, 47; median 49) years with tumors arising in inguinal lymph nodes (n=15), a neck lymph node (n=1), and undesignated lymph nodes (n=2). Most individuals presented with a painless mass or lump. Possible trauma/injury to the inguinal region was documented in 4 cases. Tumors ranged in size from 1.0 to 4.2 (mean, 3.1; median; 3.0) cm. Microscopically, the process presented as a well-circumscribed, oftentimes pseudoencapsulated nodule (n=17) or nodules (n=1). Tumors consisted of a cellular proliferation of cytologically bland, spindled cells arranged in short fascicles and whorls within a finely collagenous (n=11) or myxocollagenous (n=7) matrix. In 12 tumors, scattered fibromatosis-like fascicles of spindled cells were noted. Histologic features characteristic of the process included nuclear palisades (n=16 cases), collagenous bodies (n=15), and perinuclear intracytoplasmic hyaline globules (n=10). Mitotic activity ranged from 0 to 8 (mean, 2; median, 1) mitotic figures/50 high-powered fields with no atypical division figures identified. Immunohistochemically, all tumors tested expressed smooth muscle actin and/or muscle-specific actin (n=5, each), and nuclear β-catenin and cyclin D1 (n=8, each). The latter 2 results prompted a screening for mutations in the β-catenin gene glycogen synthase kinase-3 β phosphorylation mutational "hotspot" region in exon 3 using polymerase chain reaction amplification and Sanger sequencing. Single nucleotide substitutions leading to missense mutations at the protein level were identified in 7 of 8 (88%) analyzed tumors and are responsible for the abnormal expression of β-catenin and cyclin D1. These results demonstrate that mutational activation of the β-catenin gene is likely a pivotal event in the pathogenesis of intranodal palisaded myofibroblastoma.
Journal of Oral and Maxillofacial Pathology · 2016 · 19 citations · open access
Immunohistochemical evaluation of myofibroblasts in odontogenic cysts and tumors: A comparative study
AbstractCONTEXT: Myofibroblasts are fibroblasts with smooth muscle-like features characterized by the presence of a contractile apparatus and found in the connective tissue stroma of normal tissues such as blood vessels and lymph nodes. They are now thought to play a role in the synthesis and reorganization of extracellular matrix, which could contribute to the aggressive biologic behavior of the lesions. AIMS: To compare the mean number of stromal myofibroblasts in dentigerous cysts (DCs), keratocystic odontogenic tumor (KCOT) and ameloblastoma; and to derive a correlation between the stromal myofibroblasts and the known biologic behavior of the lesions. SETTINGS AND DESIGN: A cross-sectional immunohistochemical analysis of cases of DC, KCOT and ameloblastoma. MATERIALS AND METHODS: Twenty paraffin-embedded tissue blocks each of DC, KCOT and multicystic ameloblastoma were selected for the study and diagnosis confirmed through hematoxylin and eosin staining. Tissue sections were analyzed for the number of myofibroblasts using alpha smooth muscle actin (α-SMA) immunostaining. STATISTICAL ANALYSIS: Differences in the mean number of α-SMA positive cells in each group were analyzed using one-way ANOVA test. Intergroup comparisons of mean values of α-SMA positive cells were performed using Mann-Whitney U-test. RESULTS: Ameloblastoma showed the highest number of myofibroblasts, whereas DC showed the lowest. Among the groups, there were significant differences between the myofibroblast counts among DC and KCOT and between DC and ameloblastoma, whereas the difference in counts was not statistically significant between KCOT and ameloblastoma. A positive correlation was observed between the myofibroblast count and the known biologic behavior of the lesions. CONCLUSION: Myofibroblasts may act in close association with the epithelial cells to bring about changes in stromal microenvironment, favorable to the growth and progression of the lesion. They may be of great value in predicting the biologic behavior and growth potential of such lesions.
Polish Journal of Radiology · 2016 · 10 citations · open access
Intranodal Palisaded Myofibroblastoma: Radiological and Cytological Overview
AbstractBACKGROUND: Intranodal palisaded myofibroblastoma is a benign and very rare mesenchymal neoplasm of the lymph nodes originating from differentiated smooth muscle cells and myofibroblasts. CASE REPORT: We report a case of intranodal palisaded myofibroblastoma in an 84-year-old woman with Parkinson's disease that presented as a left inguinal mass. The diagnosis was made using ultrasound-guided fine needle aspiration biopsy and consequent cytopathological examination that included immunohistochemical analysis. Herein, we discuss the presentation of a rare intranodal palisaded myofibroblastoma with emphasis on its ultrasonographic and cytopathologic features. CONCLUSIONS: Intranodal palisaded myofibroblastoma should be considered in the differential diagnosis of inguinal lymphadenopathy and the diagnosis is possible with cytopathologic exam and immunohistochemical analysis using ultrasound-guided FNA biopsy, guiding the clinician to nodal excision rather than aggressive measures.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
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